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Aims Cardiac troponin I (cTnI) is considered a marker of myocardial necrosis. However, several studies have shown that cTnI increases also after short episodes of myocardial ischaemia. Nevertheless, it is unknown whether the changes in cTnI show differences according to the cause of myocardial ischaemia. Thus, our study aimed to evaluate cTnI response to ischaemia in patients with stable coronary artery disease (CAD), patients with microvascular angina (MVA), and transient ischaemia induced during percutaneous coronary intervention (PCI). Methods and results We studied four groups of patients: (1) patients with stable angina and obstructive CAD (coronary stenosis ≥50% and/or fractional flow reserve &amp;lt;0.80) (Group 1, n = 8); (2) patients with stable angina but no obstructive CAD and a final diagnosis of MVA according to positive intracoronary acetylcholine provocation test and/or coronary flow velocity reserve assessment with transthoracic Doppler echocardiography (Group 2, n = 20); (3) patients with stable angina and obstructive CAD undergoing PCI (Group 3, n = 10); (4) a control group of healthy subjects, with no history of cardiovascular disease (CVD) (Group 4, n = 20). Patients in groups 1, 2, and 4 underwent ECG exercise stress test (EST) according to a standard treadmill Bruce protocol. Peripheral venous blood samples were collected immediately before, at the end and 1, 3, and 24 h after test ending. Patients in group 3 underwent PCI with at least one drug-eluting stent implantation. Peripheral venous blood samples were collected immediately before, at the end and 1, 3, and 24 h after PCI ending. High-sensitivity cTnI (hs-cTnI) levels were measured by chemiluminescent microparticle immunoassay (CMIA). The main results of hs-cTnI in the four groups of patients are summarized in the table. Basal hs-cTnI serum levels were significantly higher in group 3, while there were no significant differences among groups 1, 2, and 4. Hs-cTnI serum levels significantly increased in all groups in response to the procedure (EST or PCI). A greater increase of hs-cTnI was found in group 3 (peak level at 24 h) compared to the other groups (peak level at 3 h). Furthermore, among patients undergoing EST, a significantly higher hs-cTnI increase was found in healthy subjects, compared to patients with CAD and MVA. Heart rate (HR) during stress test (both as an absolute value and predicted maximal HR for age) was the only variable statistically predictive of hs-cTnI increase during EST (HRmax: r 0.289, P 0.04; %HRmax: r 0.307; P 0.03). On the other hand, no clinical and laboratory variable was associated to hs-cTnI response after PCI. Conclusions Hs-cTnI serum levels increase after EST, both in patients with obstructive CAD and coronary microvascular dysfunction (CMD), but a similar increase is also observed in healthy subjects. More consistent hs-cTnI level increase with later peak-level is observed in patients with obstructive CAD after transient ischaemia induced during PCI.

236 Variation in cardiac troponin I serum levels after ECG exercise stress test in patients with microvascular angina